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Resp Flashcards

1
Q

the upper resp tract contains what?

A

nasopharynx oropharynx - from soft palate to epiglottis

larynx - tongue to trachea

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2
Q

what is the cribiform plate?

A

the superior portion of the nasal cavity which contains nerve endings for sense of smell - parth of the ethmoid bone.

The cribiform plate sits between the frontal and sphenoid sinus

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3
Q

name the sinuses

A

frontal, ethmoid, sphenoid, maxillary

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4
Q

the mucosa of the naso and oropharynx are supplied by which cranial nerve?

A

Cranial nerve V - the trigeminal nerve

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5
Q

which arteries supply the nasopharynx?

A

branches that run from the external carotid (maxillary and sphenopalatine)

and

the internal carotid (anterior ethmoidal from the opthalmic)

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6
Q

what is the role of the larynx?

A

separates food

protects the trachea

phonation

breathing

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7
Q

what does the arytenoid cartilage do?

A

movement is for phonation and vocalisation

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8
Q

which nerves innervate the motor function of the larynx?

A

branches of the vagus nerve:

superior laryngeal nerve (external branch)

recurrent laryngeal branch

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9
Q

sensory and autonomic innervation of the larynx?

A

branches of the vagus nerve:

superior laryngeal nerve (internal branch) above true vocal cords

recurrent laryngeal branch - below vocal cords

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10
Q

what is the narrowest point of a childs airway?

A

the crichoid cartilage (larynx)

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11
Q

what is Boyle’s law?

A

V1 x P1 = V2 x P2

volume increases so pressure decreases

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12
Q

what is the most important factor to determine recoil?

A

surface tension

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13
Q

which law’s relate to surface tension?

A

Boyle and La Place (P = 2T/r)

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14
Q

what is Dalton’s law?

A

a law stating that the pressure exerted by a mixture of gases in a fixed volume is equal to the sum of the pressures that would be exerted by each gas alone in the same volume

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15
Q

what is the intrapleural pressure normally?

A

usually around -4 mmHg but value may change

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16
Q

How do the pressures change during inspiration?

A

contraction of diaphragm and external intercostals

P pleural drops from -4 to -6 mmHg

P alveoli drops from 0 to -3 mmHg

P L (transpulmonary) is -3 mmHg - airflow goes in as this is below atmospheric pressure

PL = PA - PPL

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17
Q

How do the pressures change during expiration?

A

Insp muscles relax

P pleural rises from -6 to -4 mmHg

P alveoli rises from -3 to +3 mmHg

P L (transpulmonary) is 7 mmHg

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18
Q

What is tidal volume?

A

regular inspiration / expiration

normally about 500 mL

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19
Q

What is vital capacity?

A

maximum inhalation and maximum exhalation

about 4800 mL

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20
Q

Total lung capacity is normally what?

A

6000 mL

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21
Q

what is the residual volume?

A

the amount remaining in the lungs unable to be exhaled - about 1200 mL

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22
Q

what is the expiratory reserve volume?

A

the additional air available for forced expiration - about 1200 mL

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23
Q

what is the inspiratory reserve volume?

A

the additional volume able to be inspired above quiet breathing volume - about 3100 mL

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24
Q

what is the equation for airway resistance?

A

R airways = difference P/V (volumetric airflow)

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25
Q

what are the pressures in the pulmonary veins and arteries?

A

veins approx 9 mmHg

arteries 25/12 mmHg but varies in different areas of the lung

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26
Q

what is the bohr effect?

A

right shift in the oxygen-Hb curve making oxygen have a lower affinity for Hb

incease in H+, CO2, 2,3 DPG due to anaerobic glycolysis in RBCs

drop in pH

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27
Q

what is the haldane effect?

A

deoxyhaemoglobbin binds more readily with CO2

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28
Q

how is CO2 carried in the blood?

A

mainly as bicarbonate (90%) 5% dissolved and 5% with Hb

nb - values change depending on source

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29
Q

peripheral and central chemoreceptors detect what? and communicate via which nerves?

A

CO2 and H+ via the vagus (CNX) and glossopharyngeal nerve (CNIX)

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30
Q

what are the non-respiratory functions of the lungs?

A

helps to adapt blood volume via posture

filter for clots, fibrin and lipid droplets

defense - filtering, IgA

hormone reg - removes serotonin, converts Ang I to Ang II

Drug metabolism - cytP450

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31
Q

how do you calculate alveolar ventilation?

A

tidal volume 500 - 150 (dead space) x by RR

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32
Q

how long to RBCs spend in pulm caps? what is the diffusion time for oxygen?

A

RBC’s in caps 0.75 s

diffusion time 0.25 s

this reduces with exercise

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33
Q

what is the oxygen content of plasma?

A

0.003 mL/100 mL

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34
Q

oxygen content in blood?

A

20 mL/100mL

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35
Q

if the CO is 5L/min how much oxygen is delivered to the body.

A

1000 L/min

(20 mL/100 mL oxygen in blood x 5 for CO)

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36
Q

What % of type I and type II alveolar cells make up the alveolar wall?

A

type I = 95% of surface area

type II 5% of surface area

but type II make up 60% of actual cell numbers

** type II can become type I**

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37
Q

where do alveolar macs reside? what do they do?

A

mucus layer and the interstitium

apoptosis, immune, suppress T cells

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38
Q

what does surfactant do?

A

reduce surface tension

increase compliance

stabilse alveolar structure

prevents fluid movement into alveoli (protects diffusion distance)

activates immune system

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39
Q

which types of surfactant proteins are hydrophobic?

A

A and D hydrophilic

B and C hydrophobic (blood cold = hydrophobic)

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40
Q

what ratio is a determinant of foetal lung maturity?

A

L/S ratio lecithin and sphingomyelin

These are glycoproteins which make up part of surfactant. Amniotic fluid can be tested to assess lung maturity of the foetus.

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41
Q

surfactant is made up of what?

A

phospholipids 80% (DPCC 60% and phosphotidylglycerol/ethanolamine/inositol 20%)

neutral lipids 10%

surfactant proteins 10%

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42
Q

what does the foetal lung develop from?

A

the foregut

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43
Q

What are the 4 stages of lung development?

A

1. Pseudoglandular (wk 6-16) – looks histologically like a gland, no respiration possible

2. Canalicular (wk 16-26) – at the end respiration possible (primordial alveoli present), surfactant production begins (wk 20)

3. Terminal (wk 26-birth) – alveolar epithelium becomes thin and capillaries are in close contact.

4. Alveolar (wk32 –8 years) –alveolar ducts and sacs present, mature alveoli develop AFTER birth. New alveoli are added until age of 8 years!

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44
Q

At what stage in foetal development is surfactant production sufficient?

A

surfactant production sufficient @ wk 26-28

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45
Q

what occurs in the foetus at birth to aid in the absorption of liquid from the lungs?

A

– adrenaline activates Na+channels in type I alveolar cells

  • type II cells (vasopressin, cortisol and T3 are also involved)
  • Na+ will be removed from the liquid in alveoli and fluid follow = resorption of fluid in alveoli;

– aquaporins inserted: water channel-forming proteins

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46
Q

in the immature lung what factors exist that impede gas exchange?

A

Not conducive to gas exchange •

Thick blood gas barrier •

Low compliance •

Immature epithelial cells •

Low surfactant levels •

Small area for gas exchange •

Poorly vascularized •

High resistance to blood flow

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47
Q

what is the equation which shows the factors affecting compliance?

A

compliance = diff vol / diff pressure

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48
Q

what forces are responsible for recoil of the lungs?

A

surface tension

elastic fibres/collagen

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49
Q

what are the major inflammatory cells in asthma?

A

mast cells

eosinophils

neutrophils

Th2 cells

CD4+ cells

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50
Q

what are the major inflammatory cells in COPD?

A

neutrophils

macrophages

epithelial cells

CD8+ cells

Th2 cells

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51
Q

what are the major differences between COPD and asthma?

A

Asthma reversible, COPD not so much

SM increase - Asthma +++, COPD +

Fibrosis - Asthma +, COPD +++

Parenchymal damage - Asthma no , COPD ++

Mucus secretion - Asthma +, COPD +++

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52
Q

state the alveolar gas equation

A

pAO2 = FiO2 - (PaCO2 / 0.8)

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53
Q

what is the thickness of the blood gas barrier? what is its area?

A

0.2 micro metres

50-100 meters squared

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54
Q

in the apices of the lungs with regards to pressure ? > ? > ?

A

alveolar > arterial > venous

so low perfusion due to the alveolar pressure compressing the capillaries

V/Q ratio higher at apices

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55
Q

in the middle section of the lung with regards to pressure ? > ? > ?

A

arterial > alveolar > venous

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56
Q

in the lower portion of the lung with regards to pressure ? > ? > ?

A

arterial > venous > alveolar

so lung compliance is higher at the bases as the alveoli are already open ready to be ventialated

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57
Q

state the equation for oxygen delivery

A

Oxygen Delivery = Cardiac Output x Oxygen Content in blood

DO2 = CO x CaO2

so CO and Hb can compensate for reduced CaO2

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58
Q

how is CO2 carried in the blood?

A
  1. 10% in dissolved form (CO2 20 x more soluble than O2)
  2. 5% bound to blood proteins (mostly Hb) carbamino-haemoglobin 3.

85% forms bicarbonate in blood

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

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59
Q

what are the determinants of PaCO2

A

PaCO2 unaffected by diffusion abnormalities

PaCO2 depends on - alveolar ventilation - CO2 production (VCO2)

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60
Q

how do you calculate the A-a gradient?

A

A-a gradient = PAO2 – PaO2

Normal A-a is between 5-10 mmmHg

(possibly a bit higher if old - calculate age/4 + 4)

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61
Q

how do you calculate PAO2?

A

PAO2 = PiO2 - PaCO2/0.8 (or you can multiply by 1.25)

Where PiO2 is atmospheric O2 - vapour pressure of the FiO2 on oxygen

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62
Q

state the two different forms of shunt

A

Blood flow bypasses ventilated alveoli

Cardiac – venous blood bypasses lungs

Pulmonary – alveoli perfused but not ventilated

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63
Q

if PaCO2 rises, what is the effect on PAO2?

A

So if PaCO2 is higher… then PAO2 will be lower… so PaO2 must also be lower

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64
Q

state the components of airway defence

A

structural

innate

inflammatory

specific immune responses cell mediated responses

resp immuglobulins

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65
Q

what are the functions of nasal airflow creating turbulent flow?

A

mix air

enable greater contact with surface area

deposition of particles

change airflow direction

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66
Q

nasopharyngeal filtering is effective for what particles?

A

> 10 micro meters

partially effective for > 5 micro meters

absorption of soluble and inert gasses

mixing of air allows for inertial deposition of larger particles via impation

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67
Q

impacted particles are removed from the NP via?

A

sneezing, coughing, swallowed

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68
Q

microscopically there are two layers in the mucosa?

A

cilated mucosal layer to stick particles and sweep away top gel layer

underlying sol

latter is more water like to make sweeping more easy

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69
Q

what is the purpose of humidification in the airways?

A

moisten and warn the air.

occurs in nasal passages thanks to turbulent flow, vascular network and mucosal surfaces

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70
Q

how many airway generations are there before gas exchange occurs?

A

22-23

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71
Q

what is the mucociliary elevator?

A

continuous lining of airway with epithelial cells, trap particles > 2 micro meters and sweep upward to be coughed out or swallowed

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72
Q

what are the histological components of the conducting airways?

A

psuedostratified ciliated cells 200 cilia per cell (12-14 beats per second)

rapid clearance

  • trachea half-life 30 minutes
  • distal airways take hours
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73
Q

in the mucus layer, the top layer contains mucins. what is their function?

A

provide a sticky layer to trap particles

have carbohydrate receptors for specific interactions with microbes

enhances bacterial clearance in functional mucociliary elevator

74
Q

what is lactoferrin?

A

present in airways and binds iron to prevent it being used by microbes for growth. also protects tissues from hydroxyl free radical damage.

75
Q

what are the particle sizes and what are their methods of collection/clearance?

which size particle is the biggest problem?

76
Q

what are the non-mucinous secretions of the airways?

A

lactoferrin

lysozyme

proteases

77
Q

what are lysozymes and what is their function?

78
Q

what are proteases, what produces them and what do they do?

79
Q

what do the lungs produce to protect against bacterial proteases?

80
Q

what is the diving reflex?

81
Q

explain the cough reflex

82
Q

What 6 things are components of the innate immune system in the airways?

A
  1. PRRs which reconise PAMPs
  2. TLRs
  3. Macrophages
  4. NK cells
  5. complement
  6. surfactant
83
Q

PAMP’s are produced by what and include what types?

A

Produced only by microbes, and include:

  • lipopolysacharides on gram +
  • teichoic acids on gram -
  • mannans on yeast cells
  • unmethylated CpG motifs
  • bacterial DNA
84
Q

What are the functions of secreted vs endocytic PRRs?

A

secreted:

  • function as opsonins which activate complement and proteases eg. mannin-binding lectin, serum amyloid protein, c-reactive protein

endocytic:

  • mediate phagocytosis of microorganisms eg. marcophage mannose receptor (MMR) and macrophage scavenger receptor (MSR)
85
Q

what do signalling receptors (aka Toll like receptors) do?

A

recognise PAMP’s andd activate transduction pathways to induce:

  • inflammatory cytokines (TNF alpha, IFN alpha/beta, chemokines),
  • co-stimulate T cells,
  • signal to differentiating lymphocytes (via IL’s, TGF, IFN)
  • upregulate microbial killing (iNOS, NO)
86
Q

alveolar macs are the first line of alveolar defense, what types are there are when can they be found?

A

Pulmonary and circulating

Found in the pulmonary interstitium, lining of alveoli and airway lumen and epithelial cells

87
Q

what are the functions of alveolar macs?

A
  • signal recognition via PRRs and complement receptors
  • migration in response to ILs, IFN, cytokines
  • secretion of mediators
  • Microbe ingestion
    • via ligand interaction which is receptor specific
    • pseudopods envelop microbe
    • microbe contained in phagosome
  • microbe killing
    • oxidative
    • non-oxidative via defensins
88
Q

What to NK cells do?

A
  • interact with macs to help activate them
    • Macs + microbe = IL 12 production
    • IL 12 + TNF alpha causes NK cells to produce INY gamma
    • INF gamma activates and enhances microbial activity of macs
89
Q

what type of complement components are present in normal alveolar fluid?

A

alternate (pathogen surface antigen route)

90
Q

activation of the complement causes what?

A
  • C3b to promote phagocytoosis
  • C5a production to attract polymorphonuclear neutrophil leucocytes
  • Assembly of the C5b-C9 membrane attack complex
91
Q

Surfactant SP A and SP D are forms of what?

A

Collectins, part of innate immunity

92
Q

SP A has what functions?

A
  • faciliates mac and type II alveolar cell uptake of microbes
  • opsonises H. influenza A
  • promotes chemotaxis
  • modifies oxidant production to prevent tissue damage
93
Q

SP D does what?

A

mediates agglutination (clumping together) of gam - bacteria

deteergent effect assists in extracellular killing

94
Q

what to neutrophils produce to aid in killing?

A
  • bacericidal substances such as H2O2, superoxides, hydroxyl radicals.
  • oxygen independent substances:
    • lactoferrin
    • lysozyme
    • defensins
95
Q

what are the major differences between the type 11 and type 2 immune responses?

A
  • type 1
    • activated macs
    • involves phagocytosis and intracelllular killing
    • mediated by Th1 cells which secrete
      • IL2, IFN gamma, TNF alpha, GM-CSF
  • type 2
    • non-cytotoxic antibodies, mast cells and eosinophils
    • mediated by Th2 secreting IL 4, 5, 6 and 10
    • primitive response - allergies
96
Q

what is the primary antibody in the lungs?

A

IgA - derived from mucosal B cells mainly present in the bronchus associated lymphoid tissue

97
Q

In ABG analysis, what will tell you if there is a diffusion issue?

A

By comparing PaO2 and PAO2

98
Q

What are the normal values for pH, PaCO2, Pa O2 and Pa HCO3?

A

pH 7.40 (7.35 - 7.45)

PaCO2 40 mmHg (38 - 42)

PaO2 97 mmHg (80 - 100)

HCO3 24 mmol/L (22 - 28)

99
Q

In an academia:

what is the cause if the HCO3 is low?

Or is the CO2 is high?

A

low pH and low HCO3 = metabolic acidosis

low pH and High CO2 = respiratory acidosis

100
Q

In alkalaemia what is the causde if:

HCO3 is high?

CO2 is low?

A

high pH and high HCO3 = metabolic alkalaemia

high Ph and low CO2 = resp alkalosis

101
Q

In a respiratory acidosis, how can you tell if it is acute or chronic?

A

In acute bicarb can’t compensate so it will only rise by 1-2 per 10 mmHg increase in PaCO2

In chronic the kidneys have time to compensate so bicarb will rise by 4 per 10 mmHg increase in PaCO2

102
Q

In a metabolic acidosis what should PaCO2 drop by to compensate?

A

For each 1 of bicarb CO2 should drop by 1.4

103
Q

In metabolic alkalosis how much should CO2 change related to bicarb?

A

CO2 should rise by 0.5 to each 1 of bicarb increase

104
Q

how do you calculate for an anion gap?

A

Na - (Cl + HCO3)

Normal anion gap is 12 +/- 4

105
Q

what may cause an increased anion gap?

A
  • lactic acidosis
  • ketoacidosis
  • salicylate poisoning
  • alcohol
106
Q

Analyse the following:

pH 7.00 (7.35 - 7.45)
PaCO2 90 mmHg (38 - 42)
PaO2 35mmHg (80 - 100)
HCO3 34 mmol/L (22 - 28)

A

Resp acidosis (low pH / high CO2)

Acute as bicarb is only raised by 2 for each 10 that CO2 has risen.

Hyoxic with a normal A=a gradient = hypoventilation

108
Q

what are the histopathological changes found in asthma?

A
  • denundation of airway epithelium
  • desquamation of epithelia and fragility
  • collagen deposition beneath the basement membrane
  • mast cell degranulation
  • oedema
  • inflammatory cell infiltration
109
Q

what is the pathophysiology of asthma?

A
  • acute airway narrowing due to:
    • smooth muscle contraction
    • airway oedema
    • mucus plugging
  • chronic airway onbstruction due to:
    • smooth muscel hypertrophy
    • sub-epithelial collagen depostition
  • distal airway obstruction may lead to V/Q mismatch
110
Q

what are the three main mediators released from mast cell and their functions in asthma?

111
Q

what are the major mediators released from eosinophils and their functions in asthma?

112
Q

what do epithelial cells release in asthma?

113
Q

what do T cells release in asthma and what do they do?

A

GM-CSF, IL 3, 4, 5

all attract and enhance production eosinophils

114
Q

what difference does it make if you find either eosinophils of neutrophils in a sputum sample with regards to damage of the lung?

A

eosinophils = loss of control which may improve with corticosteroids

neutrophils = irreversible lung destruction

115
Q

in what ways are epithelia and t cell vital in inducing the late phase response in asthma?

A

they modulate the influx of inflammatory cells, release cytokines which induce the expresion of adhesion molecules - CAMs, which enable the migration on inflammatory cells into the airway walls.

116
Q

whats the difference between panacinar and centriacinar emphysema?

A

centriacinar involves the distention and destruction of alveoli in the centre of the acini, most often in the upper portions of the lung.

Panacinar involves more diffuse destruction throughout the acini, often in the lower lung.

117
Q

what changes do you find in the small airways in chronic bronchitis?

A
  • goblet cell hyperplasia
  • mucus gland dilation and hyperplasia
  • thickened basement membrane
  • fibrosis
  • squamour metaplasia
  • oedema
  • inflammatory infiltrate
  • exudate into lumen
  • hyperemia
118
Q

what is the pathophysiology of chronic bronchitis and emphysema?

A

chronic bronchitis:

  • airflow obstruction
    • mucus plugging
    • airway wall thickening
  • V/Q mismatch
  • alveolar hypoventilation

emphysema:

  • airflow obstruction due to dynamic airway collapse
  • V/Q mismatch
  • Diffusion issue due to reduced surface area
119
Q

what are the differences in the clinical pictures of pink puffers and blue bloaters?

120
Q

what are the palpable components of the larynx, and at what cervical levels are they?

A
  • hyoid bone - C3
  • thyroid cartilage - C4 and 5
  • crichoid cartilage - C6
121
Q

where are the two joints in the larynx?

A
  • the hyoid and thyroid
  • cricothyroid joint
122
Q

which muscles ADDUCT the voval cords?

which ABDUCT?

A
  • ADDUCT - closes folds and glottis
    • transverse arytenoids
    • lateral crichoarytenoids
  • ABDUCTS - opens
    • posterior cricoarytenoids
123
Q

name the intrinsic muscles of the larynx?

A

Intrinsic muscles act on the components of the larynx to change the size of the rima glottidis and vocal cords.

  • crichothyroid - tenses
  • thyroarytenoid - relaxes
  • post. crychoarytenoid - Abducts
  • lateral crychoarytenoid - adducts
  • trans and oblique arytenoids - adducts
124
Q

what is the vallecula?

what problems can it cause?

A
  • a groove at the base of the tongue between the tongue and the epiglottis
  • food/crumbs can get stuck there - cough
125
Q

what is the aryepiglottic fold?

what does it do?

A
  • covering of the muscle which runs from the epiglottis to the arytenoids
  • reduces in size when swallowing and closes over the laryngeal opening
126
Q

what makes up the quadrangular membrane?

127
Q

what is the piriform fossa?

what can happen there?

A
  • small groove on either side of the layngeal inlet where objects can get stuck
128
Q

what is the rima glottidis?

A

the opening in between the vocal cords?

129
Q

what is the conus elasticus?

A
  • sheet of ligament that runs laterally from the crichoid cartilage, superiorly and medially with the free medial edges making the TRUE VOCAL FOLDS/vocal ligaments
130
Q

what is the total inspiratory capacity derived from?

A

todal volume + inspiratory reserve

131
Q

what does vital capacity encompass?

A
  • inspiratory reserve + tidal volume + expiratory reserve volumes

so it is the total ventilatory capacity excluding the risidual volume

132
Q

what is the functional residual capacity?

A

expiratory reserve + residual capacity

133
Q

at what level of branching does airway cartilage cease?

A

at the bronchioles - approx. generation 10 onwards

134
Q

what size particles can be cleared by the mucociliary elevator?

A

>2 micrometers

135
Q

describe vesicular sounds

A
  • rustling sound
  • made by air moving through smaller airways
  • no gap between insp/exp
  • insp longer
136
Q

describe bronchial breath sounds

A
  • made by air moving thorugh trachea
  • hollow harsh sound
  • gap between insp/exp
  • exp is longer
137
Q

describe pathological changes in bronchial breath sounds

A

if heard in other areas = consolidation

decreased in pleural effusion and pneumothorax

138
Q

what causes crackles?

A
  • inspiratory sound as alvioli pop open
  • causes which make the small airways collapse (then causing them to pop open on insp) include:
    • COPD
    • oedema
    • fine crackles - fibrosis
    • coarse - bronchiectasis
139
Q

how does the nasal cavity humidify air?

what other functions does it have?

A
  • highly vascularised so blood warns the air
  • goblet cells produce mucus to moisten it
  • filters particle for impaction and clearance
  • absorbs soluble and reactive gases
140
Q

whare does gravitational preciptitation occur?

A

in the smaller bronchioles for particles 1-5 micrometers

141
Q

when does pleural rub occur (insp/exams)?

what causes it?

A

creaking/grating on exp

caused by inflammation of the pleura due to pneumonia, emphysema, pleurisy

142
Q

what are the signs of upper airway obstruction?

A
  • noisy breathing
  • stridor
  • sweating
  • agitiation
  • tachypnoea
  • tracheal tug
  • cyanosis
  • collapse
143
Q

what happens in the diving reflex?

A
  • cold or wet stimulus on face - CN V (trigeminal nerve) CN VIII (vestibulocochlear)
  • inhibits resp centre - apnea
  • activates cardiovascular centre
    • sympathetic - periph vasoconstriction to redirect blood to heart
    • parasympathetic - slows heart
  • arterial chemorecptors reinforce
144
Q

what are some causes of upper airway obstruction?

A
  • viral croup - parainfluenza often
  • epiglottitis
  • foreign body
  • bacterial tracheitis
  • diptheria - membrane formation
  • peritonsilar abcess
145
Q

what is the management for upper airway obstruction?

A
  • oxygen - humidified
  • nebulised adrenaline 5mg/5ml (croup, epiglottitis) to reduce oedema via vasoconstriction
  • remove foreign body
  • intubation
  • crichothyroidotomy
  • tracheostomy
146
Q

what are the four phases of the cough reflex?

A
  1. sensory
    • vagal pulmonary fibres sense mechanical or chemical stimulus - stim brainstem and cortex (NTS and VRG)
  2. inspiratory
    • large intake - stretch muscle = greater positive intracthoracic on expoiration.
  3. compressive
    • glottis is closed, volume remains same, intrathoracic pressure builds to >100 mmHg
  4. expiratory
    • glottis opens and air is expelled with force
147
Q

what are the 5 steps involved in virus replication?

A
  1. adsorption
    • binds to receptors on cell surface
  2. penetration
    • virus penetrates cell via pinocytosis and can release their contents into the cell, uncoating their nucleic acid.
  3. proliferation
    • viral componenets proliferate
    • synthesis of capsid and non-capsid proteins
    • nucleic acid replicates
  4. assembly
  5. release
148
Q

what is the structure of a virus?

A
  • Genome:
    • Either DNA (usually double stranded and helical) or RNA (often single stranded and sometimes segmented)
  • Capsid:
    • A shell of virus coded protein, that is closely associated with the nucleic acid – may both be referred to as nucleocapsid
    • Made of subunits – capsomers – specific to the virus species, composed of several polypeptides
    • Responsible for host attachment in non-enveloped viruses.
  • Envelope:
    • May or not be present, surrounds the capsid
    • Often forms spikes
    • host derived lipid membrane containing viral derived proteins
  • Tegument – amorphous protein layer/matrix
  • Accessory proteins
149
Q

describe the foetal circulation

150
Q

what maintans the patency of the ductus arteriosus?

A

prostoglandins PGE2 which are 5x higher in the foetus

151
Q

what are the effects of losing maternal circulation at birth?

A
  • umbilical cord stretches causing vasoconstriction of the umbilical arteries
  • this causes an increase in PVR x 2 which feeds back up the arterial system
  • aortic and LV pressure increase
152
Q

what induces the ductus arteriosus to close?

A
  • increased aortic pressure reverses flow
  • higher oxygen content causes vasoconstriction
  • closes totally within 1 week
153
Q

list the overall changes that occur at birth

A

(1) loss of umbilical circulation to placenta
(2) closure of ductus venosus
(3) closure of the foramen ovale
(4) closure of ductus arteriosus
(5) large increase in pulmonary circulation
(6) increase in RBF from decrease renal vascular resistance
(7) changes in skin blood flow

154
Q

what changes occur on the first breath?

A
  • normally pulm circuit is very high pressure in the foetus due to the fluid, hypoxia induced VC.
  • 1st breath causes
    • dilation of pulm circuit, marked decrease in resistance x 5
    • increased flow through pulm circuit
    • bolus blood to LA = closure of foramen ovale
155
Q

what initiates the first breath?

A
  • temporary hypoxia and hypercapnia due to loss of maternal circulation
  • cold
  • tactile stimulation
156
Q

where do the foetal lung buds develop from?

A

the foregut at approx 24 days gestation

outpouchings bud into two tubular structures which become the main bronchi

157
Q

what level of generation do alveoli appear?

A
  • generation 17 with the respiratory bronchioles
  • alveolar ducts appear at gen. 20-22
  • 300 million per lung
158
Q

where is surfactant produced and how is it released?

A

produced by lamellar bodies (a type of organelle) in type II alveolar cells.

it is released via exocytosis

159
Q

what stimulates the release of surfactant?

what recycles it?

A

surge in maternal glucocorticoids at birth

recylced by MACs or type II cells

160
Q

what are the major roles of surfactant?

A
  • reducing surface tension and thus increasing complaince
  • reduces fluid accumulation in alveoli
  • keeps alveoli size uniform in ventilation
161
Q

how does surfactant keep alveoli size uniform?

why is this important?

A
  • if one alveoli inflates more, as it gets larger the surfactant is more spread apart, causing its action in reducting surface tension to reduce.
  • this slows the inflation of this alveoli allowing others to catch up
  • Important as if alveoli are different sizes there would be a V/Q mismatch
162
Q

what induces surfactant production?

A
  • thyroid hormones
  • thyrotropin releasing hormone
  • corticosteroids
  • costisol very important:
    • increases in 3rd trimester
    • surges before birth
    • crosses placenta from mother
163
Q

which surfactant is absolutley essential?

A

SP-B

genetic abscence = foetal death

aids in absorption of lipids and lowers surface tension

164
Q

describe the normal V/Q ratio

A
  • Alveolar ventilation in L/min = approx 500 - 150 x RR
  • normal flow = CO 5 L/min
  • Alveolar ventilation normally approx 4 L/min
  • 4/5 = 0.8 so close to 1 which is equal
165
Q

what does a reduced V/Q ratio indicate?

A

an obstruction to ventilation with wasted perfusion

so the V/Q can reduce down to nearly 0

2/5 = 0.4

166
Q

what does a raised V/Q ratio indicate?

A

a reduction in perfusion = alveolar deadspace

167
Q

what happens to the V/Q ratio as you reach the bases of the lungs

A

it reduces due to a reduction in ventilation and higher levels of blood flow

168
Q

what are the variations in the V/Q from the apices to the bases of the lungs

A
  • apices = ↑V but ↓Q = towards infinity
  • 3rd rib = V/Q 1
  • bases = ↓V but ↑Q = towards 0
169
Q

what are the patial pressures of oxygen and CO2 in the arterial and venous circuits

A
  • Oxygen -
    • Pa = 104 mmHg
    • Pv = 40 mmHg
  • CO2 -
    • Pa = 40 mmHg
    • Pv = 45 mmHg
170
Q

what if diffusion reliant upon?

A
  • solubility of gas
  • thickness of barrier
  • surface area available
  • pressure diff
171
Q

what is the structure of adult Hb?

A
  • 2 alpha chains
  • 2 beta chains
  • each chain has a heam group with an iron molecule for oxygen binding
172
Q

what is the structure of foetal Hb?

A
  • 2 alpha chains
  • 2 gamma chains
173
Q

what is the general structure of Hb, what does this structure facilitate?

A

a quaternary structure which enable the change of shape as each O2 binds to a heam unit, making the structure more conducive to further O2 binding

174
Q

what is the PO2 in the interstium and then in the cells?

A
  • interstitium 40 mmHg
  • cells approx 23 mmHg
175
Q

what is the PCO2 in the interstitium and the cells?

A
  • interstitium 47 mmHg
  • cells 47 mmHg
176
Q

what is cyanosis?

A
  • caused by increased levels of deoxyHB which is blue in colour
  • can be detected when deoxyHb reaches approx 50g/L
  • If Hb content is normally 150g/L the 50g/L of deoxyHb = oxygenated Hb of about 67%
  • this = SaO2 of about 35mmHg
177
Q

what is the difference between peripheral and central?

A
  • peripheral = slowing of blood flow and greater oxygen extraction in the peripheries
  • central = deoxygenated blood already leaving the heart. seen in tongue or lips
178
Q

what are some causes of central cyanosis?

A
  • normal V/Q
    • altitude
    • or raised CO2
  • Abnormal V/Q
    • ↓ V/Q = ↓ ventilation = pneumonia
    • right to left shunt
    • ↓ ventilatory effort
179
Q

why does the cold cause peripheral cyanosis?

A
  • causes vasoconstriction = ↓ flow = ↑ time for oxygen extraction
180
Q

what is the APGAR?

A
  • appearance
  • pulse
  • grimace
  • activity
  • resp effort

scores from 0-2 with a total 10

score <5 at 5 minutes = neonatal hypoxia/asphyxia

score 7-10 at 5 minutes is normal

181
Q

what does pulse oximetry assess?

A
  • estimates the proportion Hb saturated with O2
  • measures the peripheral O2 saturation as a surrogate measure of tissue saturation
  • uses two waveforms of light gauge the ratio between oxy/deoxy Hb
182
Q

what are the disadvantages to pulse oximetry?

A
  • doesn’t detect hyperoxaemia
  • doesn’t measure oxygen tension
  • doesn’t measure ventilation
  • can be misleading in aneamia

Med school (13 decks)

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